Supplementary Materials

Supplementary Material for:

RIG-I/MAVS and STING signaling promote gut integrity during irradiation- and immune-mediated tissue injury

Julius C. Fischer, Michael Bscheider, Gabriel Eisenkolb, Chia-Ching Lin, Alexander Wintges, Vera Otten, Caroline A. Lindemans, Simon Heidegger, Martina Rudelius, Sébastien Monette, Kori A. Porosnicu Rodriguez, Marco Calafiore, Sophie Liebermann, Chen Liu, Stefan Lienenklaus, Siegfried Weiss, Ulrich Kalinke, Jürgen Ruland, Christian Peschel, Yusuke Shono, Melissa Docampo, Enrico Velardi, Robert R. Jenq, Alan M. Hanash, Jarrod A. Dudakov, Tobias Haas, Marcel R. M. van den Brink,* Hendrik Poeck*

*Corresponding author. Email: hendrik.poeck{at}tum.de (H.P.); m-van-den-brink{at}ski.mskcc.org (M.R.M.v.d.B.)

Published 19 April 2017, Sci. Transl. Med. 9, eaag2513 (2017)
DOI: 10.1126/scitranslmed.aag2513

This PDF file includes:

  • Materials and Methods
  • Table S1. Antibodies.
  • Fig. S1. Endogenous RIG-I/MAVS signaling reduces intestinal tissue damage caused by conditioning therapy and attenuates GVHD.
  • Fig. S2. Donor-derived T cells show enhanced alloreactivity in Mavs−/− allo-HSCT recipients.
  • Fig. S3. RIG-I ligands have to be applied before or during allo-HSCT to exert their protective effects and do not affect GVL.
  • Fig. S4. RIG-I–induced treatment effects are mediated by IFN-Is.
  • Fig. S5. RIG-I–induced IFN-Is enhance epithelial regeneration through stimulation of the ISC compartment.
  • Fig. S6. MAVS-deficient mice do not display an inherent defect in organoid formation or in the number of Paneth cells.
  • Fig. S7. TBI and IFN-stimulatory DNA induce a systemic IFN-I response, and feces-derived RNA triggers a RIG-I–dependent IFN-I response in IECs.

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